Genitourinary Infections and Sexually Transmitted Diseases



• Vaginitis is diagnosed by office-based testing.

• More prolonged antifungal therapy is indicated for women with complicated vulvovaginal candidiasis (VVC) than for those with uncomplicated disease.

• Women with normal physical examination findings and no evidence of fungal infection disclosed by microscopy are unlikely to have VVC and should not be treated empirically unless results of a vaginal yeast culture are positive.

• Cervicitis is commonly associated with bacterial vaginosis (BV), which, if not treated concurrently, leads to significant persistence of the symptoms and signs of cervicitis.

• Women with mild-to-moderate pelvic inflammatory disease (PID) can be treated as outpatients.

• Trocar drainage, with or without placement of a drain, is successful in as many as 90% of patients with PID complicated by tubo-ovarian abscess that fails to respond to antimicrobial therapy within 72 hours.

• Because false-negative results are common with herpes simplex virus (HSV) cultures, especially in patients with recurrent infections, type-specific glycoprotein G-based antibody assay tests are useful in confirming a clinical diagnosis of genital herpes.

• Suppressive treatment partially decreases symptomatic and asymptomatic viral shedding and the potential for transmission.

Genitourinary tract infections are among the most frequent disorders for which patients seek care from gynecologists. By understanding the pathophysiology of these diseases and having an effective approach to their diagnosis, physicians can institute appropriate antimicrobial therapy to treat these conditions and reduce long-term sequelae.


The Normal Vagina


Normal vaginal secretions are composed of vulvar secretions from sebaceous, sweat, Bartholin, and Skene glands; transudate from the vaginal wall; exfoliated vaginal and cervical cells; cervical mucus; endometrial and oviductal fluids; and micro-organisms and their metabolic products. The type and amount of exfoliated cells, cervical mucus, and upper genital tract fluids are determined by biochemical processes that are influenced by hormone levels (1). Vaginal secretions may increase in the middle of the menstrual cycle because of an increase in the amount of cervical mucus. These cyclic variations do not occur when oral contraceptives are used and ovulation does not occur.


The vaginal desquamative tissue is made up of vaginal epithelial cells that are responsive to varying amounts of estrogen and progesterone. Superficial cells, the main cell type in women of reproductive age, predominate when estrogen stimulation is present. Intermediate cells predominate during the luteal phase because of stimulation by progesterone. Parabasal cells predominate in the absence of either hormone, a condition that may be found in postmenopausal women who are not receiving hormonal therapy.


The normal vaginal flora is mostly aerobic, with an average of six different species of bacteria, the most common of which is hydrogen peroxide–producing lactobacilli. The microbiology of the vagina is determined by factors that affect the ability of bacteria to survive (2). These factors include vaginal pH and the availability of glucose for bacterial metabolism. The pH level of the normal vagina is lower than 4.5, which is maintained by the production of lactic acid. Estrogen-stimulated vaginal epithelial cells are rich in glycogen. Vaginal epithelial cells break down glycogen to monosaccharides, which can be converted by the cells themselves, and lactobacilli to lactic acid.


Normal vaginal secretions are floccular in consistency, white in color, and usually located in the dependent portion of the vagina (posterior fornix). Vaginal secretions can be analyzed by a wet-mount preparation. A sample of vaginal secretions is suspended in 0.5 mL of normal saline in a tube, transferred to a slide, covered with a slip, and assessed by microscopy. Some clinicians prefer to prepare slides by suspending secretions in saline placed directly on the slide. Secretions should not be placed on the slide without saline because this method causes drying of the vaginal secretions and does not result in a well-suspended preparation. Microscopy of normal vaginal secretions reveals many superficial epithelial cells, few white blood cells (less than 1 per epithelial cell), and few, if any, clue cells. Clue cells are superficial vaginal epithelial cells with adherent bacteria, usually Gardnerella vaginalis, which obliterates the crisp cell border when visualized microscopically. Potassium hydroxide 10% (KOH) may be added to the slide, or a separate preparation can be made, to examine the secretions for evidence of fungal elements. The results are negative in women with normal vaginal microbiology. Gram stain reveals normal superficial epithelial cells and a predominance of gram-positive rods (lactobacilli).


Vaginal Infections


Bacterial Vaginosis


Bacterial vaginosis (BV) is an alteration of normal vaginal bacterial flora that results in the loss of hydrogen peroxide–producing lactobacilli and an overgrowth of predominantly anaerobic bacteria (3,4). The most common form of vaginitis in the United States is BV (5). Anaerobic bacteria can be found in less than 1% of the flora of normal women. In women with BV, however, the concentration of anaerobes, and G. vaginalis and Mycoplasma hominis, is 100 to 1,000 times higher than in normal women. Lactobacilli are usually absent.


It is not known what triggers the disturbance of normal vaginal flora. It is postulated that repeated alkalinization of the vagina, which occurs with frequent sexual intercourse or use of douches, plays a role. After normal hydrogen peroxide–producing lactobacilli disappear, it is difficult to reestablish normal vaginal flora, and recurrence of BV is common.


Numerous studies show an association of BV with significant adverse sequelae. Women with BV are at increased risk for pelvic inflammatory disease (PID), postabortal PID, postoperative cuff infections after hysterectomy, and abnormal cervical cytology (6–9). Pregnant women with BV are at risk for premature rupture of the membranes, preterm labor and delivery, chorioamnionitis, and postcesarean endometritis (10,11). In women with BV who are undergoing surgical abortion or hysterectomy, perioperative treatment with metronidazole eliminates this increased risk (12,13).


Diagnosis


Office-based testing is required to diagnose BV. It is diagnosed on the basis of the following findings (14):



1. A fishy vaginal odor, which is particularly noticeable following coitus, and vaginal discharge are present.

2. Vaginal secretions are gray and thinly coat the vaginal walls.

3. The pH of these secretions is higher than 4.5 (usually 4.7 to 5.7).

4. Microscopy of the vaginal secretions reveals an increased number of clue cells, and leukocytes are conspicuously absent. In advanced cases of BV, more than 20% of the epithelial cells are clue cells.

5. The addition of KOH to the vaginal secretions (the “whiff” test) releases a fishy, aminelike odor.

Clinicians who are unable to perform microscopy should use alternative diagnostic tests such as a pH and amines test card, detection of G. vaginalis ribosomal RNA, or Gram stain (15). Culture of G. vaginalis is not recommended as a diagnostic tool because of its lack of specificity.


Treatment


Ideally, treatment of BV should inhibit anaerobes but not vaginal lactobacilli. The following treatments are effective:



1. Metronidazole, an antibiotic with excellent activity against anaerobes but poor activity against lactobacilli, is the drug of choice for the treatment of BV. A dose of 500 mg administered orally twice a day for 7 days should be used. Patients should be advised to avoid using alcohol during treatment with oral metronidazole and for 24 hours thereafter.

2. Metronidazole gel, 0.75%, one applicator (5 g) intravaginally once daily for 5 days, may also be prescribed.

The overall cure rates range from 75% to 84% with the aforementioned regimens (16). Clindamycin in the following regimens is effective in treating BV:



1. Clindamycin ovules, 100 mg, intravaginally once at bedtime for 3 days

2. Clindamycin bioadhesive cream, 2%, 100 mg intravaginally in a single dose

3. Clindamycin cream, 2%, one applicator full (5 g) intravaginally at bedtime for 7 days

4. Clindamycin, 300 mg, orally twice daily for 7 days

Many clinicians prefer intravaginal treatment to avoid systemic side effects such as mild to moderate gastrointestinal upset and unpleasant taste. Treatment of the male sexual partner does not improve therapeutic response and therefore is not recommended (16).


Trichomonas Vaginitis


Trichomonas vaginitis is caused by the sexually transmitted, flagellated parasite, Trichomonas vaginalis. The transmission rate is high; 70% of men contract the disease after a single exposure to an infected woman, which suggests that the rate of male-to-female transmission is even higher. The parasite, which exists only in trophozoite form, is an anaerobe that has the ability to generate hydrogen to combine with oxygen to create an anaerobic environment. It often accompanies BV, which can be diagnosed in as many as 60% of patients with trichomonas vaginitis (17).


Diagnosis


Local immune factors and inoculum size influence the appearance of symptoms. Symptoms and signs may be much milder in patients with small inocula of trichomonads, and trichomonas vaginitis often is asymptomatic (17,18).



1. Trichomonas vaginitis is associated with a profuse, purulent, malodorous vaginal discharge that may be accompanied by vulvar pruritus.

2. A purulent vaginal discharge may exude from the vagina.

3. In patients with high concentrations of organisms, a patchy vaginal erythema and colpitis macularis (“strawberry” cervix) may be observed.

4. The pH of the vaginal secretions is usually higher than 5.0.

5. Microscopy of the secretions reveals motile trichomonads and increased numbers of leukocytes.

6. Clue cells may be present because of the common association with BV.

7. The whiff test may be positive.

Morbidity associated with trichomonal vaginitis may be related to BV. Patients with trichomonas vaginitis are at increased risk for postoperative cuff cellulitis following hysterectomy (8). Pregnant women with trichomonas vaginitis are at increased risk for premature rupture of the membranes and preterm delivery. Because of the sexually transmitted nature of trichomonas vaginitis, women with this infection should be tested for other sexually transmitted diseases (STDs), particularly Neisseria gonorrhoeae and Chlamydia trachomatis. Serologic testing for syphilis and HIV infection should be considered.


Treatment


The treatment of trichomonal vaginitis can be summarized as follows:



1. Metronidazole is the drug of choice for treatment of vaginal trichomoniasis. Both a single-dose (2 g orally) and a multidose (500 mg twice daily for 7 days) regimen are highly effective and have cure rates of about 95%.

2. The sexual partner should be treated.

3. Metronidazole gel, although effective for the treatment of BV, should not be used for the treatment of vaginal trichomoniasis.

4. Women who do not respond to initial therapy should be treated again with metronidazole, 500 mg, twice daily for 7 days. If repeated treatment is not effective, the patient should be treated with a single 2-g dose of metronidazole once daily for 5 days or tinidazole, 2 g, in a single dose for 5 days.

5. Patients who do not respond to repeated treatment with metronidazole or tinidazole and for whom the possibility of reinfection is excluded should be referred for expert consultation. In these uncommon refractory cases, an important part of management is to obtain cultures of the parasite to determine its susceptibility to metronidazole and tinidazole.

Vulvovaginal Candidiasis


An estimated 75% of women experience at least one episode of vulvovaginal candidiasis (VVC) during their lifetimes (19). Nearly 45% of women will experience two or more episodes (20). Few are plagued with a chronic, recurrent infection. Candida albicans is responsible for 85% to 90% of vaginal yeast infections. Other species of Candida, such as C. glabrata and C. tropicalis, can cause vulvovaginal symptoms and tend to be resistant to therapy. Candida are dimorphic fungi existing as blastospores, which are responsible for transmission and asymptomatic colonization, and as mycelia, which result from blastospore germination and enhance colonization and facilitate tissue invasion. The extensive areas of pruritus and inflammation often associated with minimal invasion of the lower genital tract epithelial cells suggest that an extracellular toxin or enzyme may play a role in the pathogenesis of this disease. A hypersensitivity phenomenon may be responsible for the irritative symptoms associated with VVC, especially for patients with chronic, recurrent disease. Patients with symptomatic disease usually have an increased concentration of these micro-organisms (>104 per mL) compared with asymptomatic patients (<103 per mL) (21).


Factors that predispose women to the development of symptomatic VVC include antibiotic use, pregnancy, and diabetes (22–25). Pregnancy and diabetes are associated with a qualitative decrease in cell-mediated immunity, leading to a higher incidence of candidiasis.


It is helpful to categorize women with VVC as having either uncomplicated or complicated disease (Table 18.1)


Table 18.1 Classification of Vulvovaginal Candidiasis




















Uncomplicated Complicated
Sporadic or infrequent in occurrence Recurrent symptoms
Mild to moderate symptoms Severe symptoms
Likely to be Candida albicans Non-albicans Candida
Immunocompetent women Immunocompromised, e.g., diabetic women
From Sobel JD, Faro S, Force RW, et al. Vulvovaginal candidiasis: epidemiologic, diagnostic, and therapeutic considerations. Am J Obstet Gynecol 1998;178:203–211.

Diagnosis


The symptoms of VVC consist of vulvar pruritus associated with a vaginal discharge that typically resembles cottage cheese.



1. The discharge can vary from watery to homogeneously thick. Vaginal soreness, dyspareunia, vulvar burning, and irritation may be present. External dysuria (“splash” dysuria) may occur when micturition leads to exposure of the inflamed vulvar and vestibular epithelium to urine. Examination reveals erythema and edema of the labia and vulvar skin. Discrete pustulopapular peripheral lesions may be present. The vagina may be erythematous with an adherent, whitish discharge. The cervix appears normal.

2. The pH of the vagina in patients with VVC is usually normal (<4.5).

3. Fungal elements, either budding yeast forms or mycelia, appear in as many as 80% of cases. The results of saline preparation of the vaginal secretions usually are normal, although there may be a slight increase in the number of inflammatory cells in severe cases.

4. The whiff test is negative.

5. A presumptive diagnosis can be made in the absence of fungal elements confirmed by microscopy if the pH and the results of the saline preparation evaluations are normal and the patient has increased erythema based on examination of the vagina or vulva. A fungal culture is recommended to confirm the diagnosis. Conversely, women with a normal physical examination findings and no evidence of fungal elements disclosed by microscopy are unlikely to have VVC and should not be empirically treated unless a vaginal yeast culture is positive.

Treatment


The treatment of VVC is summarized as follows:



1. Topically applied azole drugs are the most commonly available treatment for VVC and are more effective than nystatin (16) (Table 18.2). Treatment with azoles results in relief of symptoms and negative cultures in 80% to 90% of patients who have completed therapy. Symptoms usually resolve in 2 to 3 days. Short-course regimens up to 3 days are recommended. Although the shorter period of therapy implies a shortened duration of treatment, the short-course formulations have higher concentrations of the antifungal agent, causing an inhibitory concentration in the vagina that persists for several days.

Table 18.2 Vulvovaginal Candidiasis—Topical Treatment Regimens































Butoconazole


   2% cream, 5 g intravaginally for 3 daysa,b

   2% cream, 5 g BI-BSR, single intravaginal applicationa
Clotrimazole


   1% cream, 5 g intravaginally for 7–14 daysa,b

   100-mg vaginal tablet for 7 daysa,b

   100-mg vaginal tablet, two tablets for 3 daysa

   500-mg vaginal tablet, single dosea
Miconazole


   2% cream, 5 g intravaginally for 7 daysa,b

   200-mg vaginal suppository for 3 daysa

   100-mg vaginal suppository for 7 daysa,b
Nystatin


   100,000-U vaginal tablet, one tablet for 14 days
Tioconazole


   6.5% ointment, 5 g intravaginally, single dosea
Terconazole


   0.4% cream, 5 g intravaginally for 7 daysa

   0.8% cream, 5 g intravaginally for 3 daysa

   80-mg suppository for 3 daysa

aOil-based, may weaken latex condoms.


bAvailable as over-the-counter preparation.

Adapted from Centers for Disease Control and Prevention. The sexually transmitted diseases treatment guidelines. MMWR 2006;55:[RR-11]:1–94.

2. The oral antifungal agent, fluconazole, used in a single 150-mg dose, is recommended for the treatment of VVC. It appears to have equal efficacy when compared with topical azoles in the treatment of mild to moderate VVC (26). Patients should be advised that their symptoms will persist for 2 to 3 days so they will not expect additional treatment.

3. Women with complicated VVC (Table 18.1) benefit from an additional 150-mg dose of fluconazole given 72 hours after the first dose. Patients with complications can be treated with a more prolonged topical regimen lasting 10 to 14 days. Adjunctive treatment with a weak topical steroid, such as 1% hydrocortisone cream, may be helpful in relieving some of the external irritative symptoms.

Recurrent Vulvovaginal Candidiasis


A small number of women develop recurrent VVC (RVVC), defined as four or more episodes in a year. These women experience persistent irritative symptoms of the vestibule and vulva. Burning replaces itching as the prominent symptom in patients with RVVC. The diagnosis should be confirmed by direct microscopy of the vaginal secretions and by fungal culture. Many women with RVVC presume incorrectly they have a chronic yeast infection. Many of these patients have chronic atopic dermatitis or atrophic vulvovaginitis.


The treatment of patients with RVVC consists of inducing a remission of chronic symptoms with fluconazole (150 mg every 3 days for three doses). Patients should be maintained on a suppressive dose of this agent (fluconazole, 150 mg weekly) for 6 months. On this regimen, 90% of women with RVVC will remain in remission. After suppressive therapy, approximately half will remain asymptomatic. Recurrence will occur in the other half and should prompt reinstitution of suppressive therapy (27).


Inflammatory Vaginitis


Desquamative inflammatory vaginitis is a clinical syndrome characterized by diffuse exudative vaginitis, epithelial cell exfoliation, and a profuse purulent vaginal discharge (28). The cause of inflammatory vaginitis is unknown, but Gram stain findings reveal a relative absence of normal long gram-positive bacilli (lactobacilli) and their replacement with gram-positive cocci, usually streptococci. Women with this disorder have a purulent vaginal discharge, vulvovaginal burning or irritation, and dyspareunia. A less frequent symptom is vulvar pruritus. Vaginal erythema is present, and there may be an associated vulvar erythema, vulvovaginal ecchymotic spots, and colpitis macularis. The pH of the vaginal secretions is uniformly higher than 4.5 in these patients.


Initial therapy is the use of 2% clindamycin cream, one applicator full (5 g) intravaginally once daily for 7 days. Relapse occurs in about 30% of patients, who should be retreated with intravaginal 2% clindamycin cream for 2 weeks. When relapse occurs in postmenopausal patients, supplementary hormonal therapy should be considered (28).


Atrophic Vaginitis


Estrogen plays an important role in the maintenance of normal vaginal ecology. Women undergoing menopause, either naturally or secondary to surgical removal of the ovaries, may develop inflammatory vaginitis, which may be accompanied by an increased, purulent vaginal discharge. In addition, they may have dyspareunia and postcoital bleeding resulting from atrophy of the vaginal and vulvar epithelium. Examination reveals atrophy of the external genitalia, along with a loss of the vaginal rugae. The vaginal mucosa may be somewhat friable in areas. Microscopy of the vaginal secretions shows a predominance of parabasal epithelial cells and an increased number of leukocytes.


Atrophic vaginitis is treated with topical estrogen vaginal cream. Use of 1 g of conjugated estrogen cream intravaginally each day for 1 to 2 weeks generally provides relief. Maintenance estrogen therapy, either topical or systemic, should be considered to prevent recurrence of this disorder.


Cervicitis


The cervix is made up of two different types of epithelial cells: squamous epithelium and glandular epithelium. The cause of cervical inflammation depends on the epithelium affected. The ectocervical epithelium can become inflamed by the same micro-organisms that are responsible for vaginitis. In fact, the ectocervical squamous epithelium is an extension of and is continuous with the vaginal epithelium. Trichomonas, candida, and herpes simplex virus (HSV) can cause inflammation of the ectocervix. Conversely, N. gonorrhoeae and C. trachomatis infect only the glandular epithelium (29).


Diagnosis


The diagnosis of cervicitis is based on the finding of a purulent endocervical discharge, generally yellow or green in color and referred to as “mucopus” (30).



1. After removal of ectocervical secretions with a large swab, a small cotton swab is placed into the endocervical canal and the cervical mucus is extracted. The cotton swab is inspected against a white or black background to detect the green or yellow color of the mucopus. In addition, the zone of ectopy (glandular epithelium) is friable or easily induced to bleed. This characteristic can be assessed by touching the ectropion with a cotton swab or spatula.
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Jul 2, 2016 | Posted by in GYNECOLOGY | Comments Off on Genitourinary Infections and Sexually Transmitted Diseases

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